A new study suggests that our feelings in our lifetime can affect our children.
Dr. Halabe Bucay suggests that a wide range of chemicals that our brain generates when we are in different moods could affect 'germ cells' (eggs and sperm), the cells that ultimately produce the next generation. Such natural chemicals could affect the way that specific genes are expressed in the germ cells, and hence how a child develops.
In his article in the latest issue of Bioscience Hypotheses, Dr Alberto Halabe Bucay of Research Center Halabe and Darwich, Mexico, suggested that the hormones and chemicals resulting from happiness, depression and other mental states can affect our eggs and sperm, resulting in lasting changes in our children at the time of their conception.
Brain chemicals such as endorphins, and drugs, such as marijuana and heroin are known to have significant effects on sperm and eggs, altering the patterns of genes that are active in them.
"It is well known, of course, that parental behavior affects children, and that the genes that a child gets from its parents help shape that child's character." said Dr. Halabe Bucay. "My paper suggests a way that the parent's psychology before conception can actually affect the child's genes."
"This is an intriguing idea" commented Dr. William Bains, Editor of Bioscience Hypotheses. "We wanted to publish it to see what other scientists thought, and whether others had data that could support or disprove it. That is what our journal is for, to stimulate debate about new ideas, the more groundbreaking, the better."
Showing posts with label Research. Show all posts
Showing posts with label Research. Show all posts
Monday, May 18, 2009
Sunday, May 17, 2009
How Oil Gets Stuck Underground In Inaccessible Places
It is a mystery to many people why the world is running out of oil when most of the world’s oilfields have only been half emptied. However some of the oil that has been located is trapped as droplets of oil in small cavities in the surrounding rock or is stuck to the walls of the underground cavity and cannot be accessed by the techniques currently used in the oil industry.
Now, new research may have come up with an explanation as to where and how North Sea oil clings to underground rocks. This explanation could turn out to be the first step on the way to developing improved oil production techniques with the intent of increasing oil production from Danish oil fields.
A research group at the Nano-Science Center, part of the Institute of Chemistry at University of Copenhagen has investigated drill cores collected from North Sea oil fields using an atomic force microscope. Their investigations show that the spaces which contain oil have totally different surface qualities than expected from our knowledge of the minerals which make up the rock. The rocks which contain oil in the Danish part of the North Sea are primarily chalk – the same type of rock that the cliffs of Stevns and Møns are made of. Assistant Professor Tue Hassenkam lead the research, whose preliminary results were published in the respected scientific publication PNAS (Proceedings of the National Academy of Sciences) this week. He says that this is the first time that investigations of this type have been carried out on chalk from an oil field in the North Sea.
'Previous investigations were carried out on the surface properties of pure mineral crystals. But our investigation has shown that this chalk has a different and more complex structure' says Tue Hassenkam.
The oil bearing layers in the subsurface are reminiscent of a sponge. The oil "hides" in tiny pores and gaps and only some of the oil can be pressed out of the chalk and into the borehole by injecting water into the chalk layer. The rest is left behind as small droplets of oil surrounded by water either in small gaps in the rock or stuck to the walls of the pores. The chalk particles ought to repel oil if they act like particles of the mineral calcite, which chalk is almost 100% made up of. However the new investigations, carried out with a particularly powerful microscope, have shown that the surfaces of the pores in the chalk are partially covered in a material which oil can stick to. Ass. Prof. Hassenkam believes that the surprising behaviour of the material in the surface of the chalk can be explained by studying how the chalk was formed.
'Chalk is actually the casings of ancient algae. The algae gave their cases a type of "surface coating" to make them resistant to water. And it is probably this surface coating that we can see in action here, even 60 million years later' according to Ass. Prof. Hassenkam.
If we can manage to squeeze even a few percent more oil out of the seabed under the North Sea it could be worth millions of Danish crowns (DKK) for Denmark. Therefore Mærsk Oil and Gas AS on behalf of DUC (Dansk Undergrunds Consortium) along with Danish National Advanced Technology Foundation are supporting a project being carried out by Professor Susan Stipps' research group – the so-called Nano-Chalk Venture, which has been ongoing for the last two years. Tue Hassenkam originally became interested in chalk because he found the algae casings so beautiful. Today, after a year's work in front of a microscope, he is glad that his work also has a practical application. An understanding of how the oil clings to the chalk can possibly help develop a method to release it. And that will be the second part of the Nano-Chalk Venture.
Now, new research may have come up with an explanation as to where and how North Sea oil clings to underground rocks. This explanation could turn out to be the first step on the way to developing improved oil production techniques with the intent of increasing oil production from Danish oil fields.
A research group at the Nano-Science Center, part of the Institute of Chemistry at University of Copenhagen has investigated drill cores collected from North Sea oil fields using an atomic force microscope. Their investigations show that the spaces which contain oil have totally different surface qualities than expected from our knowledge of the minerals which make up the rock. The rocks which contain oil in the Danish part of the North Sea are primarily chalk – the same type of rock that the cliffs of Stevns and Møns are made of. Assistant Professor Tue Hassenkam lead the research, whose preliminary results were published in the respected scientific publication PNAS (Proceedings of the National Academy of Sciences) this week. He says that this is the first time that investigations of this type have been carried out on chalk from an oil field in the North Sea.
'Previous investigations were carried out on the surface properties of pure mineral crystals. But our investigation has shown that this chalk has a different and more complex structure' says Tue Hassenkam.
The oil bearing layers in the subsurface are reminiscent of a sponge. The oil "hides" in tiny pores and gaps and only some of the oil can be pressed out of the chalk and into the borehole by injecting water into the chalk layer. The rest is left behind as small droplets of oil surrounded by water either in small gaps in the rock or stuck to the walls of the pores. The chalk particles ought to repel oil if they act like particles of the mineral calcite, which chalk is almost 100% made up of. However the new investigations, carried out with a particularly powerful microscope, have shown that the surfaces of the pores in the chalk are partially covered in a material which oil can stick to. Ass. Prof. Hassenkam believes that the surprising behaviour of the material in the surface of the chalk can be explained by studying how the chalk was formed.
'Chalk is actually the casings of ancient algae. The algae gave their cases a type of "surface coating" to make them resistant to water. And it is probably this surface coating that we can see in action here, even 60 million years later' according to Ass. Prof. Hassenkam.
If we can manage to squeeze even a few percent more oil out of the seabed under the North Sea it could be worth millions of Danish crowns (DKK) for Denmark. Therefore Mærsk Oil and Gas AS on behalf of DUC (Dansk Undergrunds Consortium) along with Danish National Advanced Technology Foundation are supporting a project being carried out by Professor Susan Stipps' research group – the so-called Nano-Chalk Venture, which has been ongoing for the last two years. Tue Hassenkam originally became interested in chalk because he found the algae casings so beautiful. Today, after a year's work in front of a microscope, he is glad that his work also has a practical application. An understanding of how the oil clings to the chalk can possibly help develop a method to release it. And that will be the second part of the Nano-Chalk Venture.
High Blood Pressure Could Be Caused By A Common Virus
A new study suggests for the first time that cytomegalovirus (CMV), a common viral infection affecting between 60 and 99 percent of adults worldwide, is a cause of high blood pressure, a leading risk factor for heart disease, stroke and kidney disease.
Led by researchers at Beth Israel Deaconess Medical Center (BIDMC) and published in the May 15, 2009 issue of PLoS Pathogens, the findings further demonstrate that, when coupled with other risk factors for heart disease, the virus can lead to the development of atherosclerosis, or hardening of the arteries.
"CMV infects humans all over the world," explains co-senior author Clyde Crumpacker, MD, an investigator in the Division of Infectious Diseases at BIDMC and Professor of Medicine at Harvard Medical School. "This new discovery may eventually provide doctors with a whole new approach to treating hypertension, with anti-viral therapies or vaccines becoming part of the prescription."
A member of the herpes virus family, CMV affects all age groups and is the source of congenital infection, mononucleosis, and severe infection in transplant patients. By the age of 40, most adults will have contracted the virus, though many will never exhibit symptoms. Once it has entered the body, CMV is usually there to stay, remaining latent until the immune system is compromised, when it then reemerges.
Previous epidemiological studies had determined that the CMV virus was linked to restenosis in cardiac transplant patients, a situation in which the heart's arteries "reblock." The virus had also been linked to the development of atherosclerosis, the hardening of the heart's arteries. But, in both cases, the mechanism behind these developments remained a mystery. This new study brought together a team of researchers from a variety of disciplines – infectious diseases, cardiology, allergy and pathology – to look more closely at the issue.
"By combining the insights of investigators from different medical disciplines, we were able to measure effects of a viral infection that may have been previously overlooked," explains Crumpacker.
In the first portion of the study, the scientists examined four groups of laboratory mice. Two groups of animals were fed a standard diet and two groups were fed a high cholesterol diet. After a period of four weeks, one standard diet mouse group and one high-cholesterol diet mouse group were infected with the CMV virus.
Six weeks later, the animals' blood pressures were measured by the cardiology team using a small catheter inserted in the mouse carotid artery. Among the mice fed a standard diet, the CMV-infected mice had increased blood pressure compared with the uninfected group. But even more dramatically, 30 percent of the CMV-infected mice that were fed a high-cholesterol diet not only exhibited increased blood pressure, but also showed signs of having developed atherosclerosis.
"This strongly suggests that the CMV infection and the high-cholesterol diet might be working together to cause atherosclerosis," says Crumpacker. In order to find out how and why this was occurring, the investigators went on to conduct a series of cell culture experiments.
Their first analysis demonstrated that CMV stimulated production of three different inflammatory cytokines – IL6, TNF, and MCP1 – in the infected mice, an indication that the virus was causing inflammation to vascular cells and other tissues.
A second analysis found that infection of a mouse kidney cell line with murine CMV led to an increase in expression of the renin enzyme, which has been known to activate the renin-angiotensin system and lead to high blood pressure. Clinical isolates of human CMV in cultured blood vessel cells also produced increased renin expression.
"Viruses have the ability to turn on human genes and, in this case, the CMV virus is enhancing expression of renin, an enzyme directly involved in causing high blood pressure," says Crumpacker. When the scientists inactivated the virus through the use of ultraviolet light, renin expression did not increase, suggesting that actively replicating virus was causing the increase in renin.
In their final experiments, the researchers demonstrated that the protein angiotensin 11 was also increased in response to infection with CMV. "Increased expression of both renin and angiotensin 11 are important factors in hypertension in humans," says Crumpacker. "What our study seems to indicate is that a persistent viral infection in the vessels' endothelial cells is leading to increased expression of inflammatory cytokines, renin and angiotensin 11, which are leading to increased blood pressure."
According to recent figures from the American Heart Association, one in three U.S. adults has high blood pressure, and because there are no known symptoms, nearly one-third of these individuals are unaware of their condition. Often dubbed "the silent killer," uncontrolled high blood pressure can lead to stroke, heart attack, heart failure or kidney failure, notes Crumpacker.
"We found that CMV infection alone led to an increase in high blood pressure, and when combined with a high-cholesterol diet, the infection actually induced atherosclerosis in a mouse aorta," says Crumpacker. "This suggests that further research needs to be directed at viral causes of vascular injury. Some cases of hypertension might be treated or prevented by antiviral therapy or a vaccine against CMV."
This study was funded by grants from the National Heart, Lung and Blood Institute of the National Institutes of Health.
Led by researchers at Beth Israel Deaconess Medical Center (BIDMC) and published in the May 15, 2009 issue of PLoS Pathogens, the findings further demonstrate that, when coupled with other risk factors for heart disease, the virus can lead to the development of atherosclerosis, or hardening of the arteries.
"CMV infects humans all over the world," explains co-senior author Clyde Crumpacker, MD, an investigator in the Division of Infectious Diseases at BIDMC and Professor of Medicine at Harvard Medical School. "This new discovery may eventually provide doctors with a whole new approach to treating hypertension, with anti-viral therapies or vaccines becoming part of the prescription."
A member of the herpes virus family, CMV affects all age groups and is the source of congenital infection, mononucleosis, and severe infection in transplant patients. By the age of 40, most adults will have contracted the virus, though many will never exhibit symptoms. Once it has entered the body, CMV is usually there to stay, remaining latent until the immune system is compromised, when it then reemerges.
Previous epidemiological studies had determined that the CMV virus was linked to restenosis in cardiac transplant patients, a situation in which the heart's arteries "reblock." The virus had also been linked to the development of atherosclerosis, the hardening of the heart's arteries. But, in both cases, the mechanism behind these developments remained a mystery. This new study brought together a team of researchers from a variety of disciplines – infectious diseases, cardiology, allergy and pathology – to look more closely at the issue.
"By combining the insights of investigators from different medical disciplines, we were able to measure effects of a viral infection that may have been previously overlooked," explains Crumpacker.
In the first portion of the study, the scientists examined four groups of laboratory mice. Two groups of animals were fed a standard diet and two groups were fed a high cholesterol diet. After a period of four weeks, one standard diet mouse group and one high-cholesterol diet mouse group were infected with the CMV virus.
Six weeks later, the animals' blood pressures were measured by the cardiology team using a small catheter inserted in the mouse carotid artery. Among the mice fed a standard diet, the CMV-infected mice had increased blood pressure compared with the uninfected group. But even more dramatically, 30 percent of the CMV-infected mice that were fed a high-cholesterol diet not only exhibited increased blood pressure, but also showed signs of having developed atherosclerosis.
"This strongly suggests that the CMV infection and the high-cholesterol diet might be working together to cause atherosclerosis," says Crumpacker. In order to find out how and why this was occurring, the investigators went on to conduct a series of cell culture experiments.
Their first analysis demonstrated that CMV stimulated production of three different inflammatory cytokines – IL6, TNF, and MCP1 – in the infected mice, an indication that the virus was causing inflammation to vascular cells and other tissues.
A second analysis found that infection of a mouse kidney cell line with murine CMV led to an increase in expression of the renin enzyme, which has been known to activate the renin-angiotensin system and lead to high blood pressure. Clinical isolates of human CMV in cultured blood vessel cells also produced increased renin expression.
"Viruses have the ability to turn on human genes and, in this case, the CMV virus is enhancing expression of renin, an enzyme directly involved in causing high blood pressure," says Crumpacker. When the scientists inactivated the virus through the use of ultraviolet light, renin expression did not increase, suggesting that actively replicating virus was causing the increase in renin.
In their final experiments, the researchers demonstrated that the protein angiotensin 11 was also increased in response to infection with CMV. "Increased expression of both renin and angiotensin 11 are important factors in hypertension in humans," says Crumpacker. "What our study seems to indicate is that a persistent viral infection in the vessels' endothelial cells is leading to increased expression of inflammatory cytokines, renin and angiotensin 11, which are leading to increased blood pressure."
According to recent figures from the American Heart Association, one in three U.S. adults has high blood pressure, and because there are no known symptoms, nearly one-third of these individuals are unaware of their condition. Often dubbed "the silent killer," uncontrolled high blood pressure can lead to stroke, heart attack, heart failure or kidney failure, notes Crumpacker.
"We found that CMV infection alone led to an increase in high blood pressure, and when combined with a high-cholesterol diet, the infection actually induced atherosclerosis in a mouse aorta," says Crumpacker. "This suggests that further research needs to be directed at viral causes of vascular injury. Some cases of hypertension might be treated or prevented by antiviral therapy or a vaccine against CMV."
This study was funded by grants from the National Heart, Lung and Blood Institute of the National Institutes of Health.
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